| Hyponatremia is when serum sodium is less than or equal to 135mmol/L. Hyponatremia is common in the ascites of liver cirrhosis. Combining the domestic reports of China, the incidence rate of liver cirrhosis ascites complicated hyponatremia is 50~60%, 30% by a series of foreign reports. The hyponatremia of liver cirrhosis ascites has no specific clinical manifestation, and its symptoms have something to do with complication, severity of hyponatremia, age, sex, etc. Hyponatremia has two cases, without symptoms or manifests itself, for example nausea, debility, disorientation, headache, lethargy, blurred vision, even encephalopathy including mind confusing, delire, epileptic attack, etc. People often misinterpret these as hepatic coma. When seurm sodium is less than or equal to 115mmol/L, its clinical manifestations (debility, headache, muscle convulsion, apthy, lethargy, mental subnormality, delirium, convulsion, coma) are clear, and even low natrium encephalopathy lead to cardiorespiratory arrest. When liver cirrhosis complicated acute low natrium syndrome (ALNS), its clinical manifestations are often nausea, vomiting, debility, etc. And severe subjects have symptoms of unorientation, blurred vision, coma, and peripheral circulatory failure. When serum sodium is less than or equal to 135mmol/L and osmotic pressure of plasma is more than 280mmol/L, it may be regarded as pseudo-hyponatremia. The reasons may be related to hyperglycemia, hyperlipemia, etc. The grading of hyponatremia is the light hyponatremia when serum sodium is 130~135mmol/L, the middle hyponatremia when serum sodium is 125~130mmol/L and the severe hyponatremia when serum sodium is less than or equal to 125mmol/L.Vasopressin (VP) can regulate the concentration of urine in medulls interna of kidney, and increase the permeability to water in collecting duct. In liver cirrhosis, the secretion of VP is stimulated by non-osmolarity, for the change of hemorrheology, including the decrease of central hypovolemia and the increase of peripheral vascular resistance and the decrease of effective blood volume leads to non-osmolarity secretion of VP. Although plasma osmotic pressure decreased, stimulation of nonosmolari- ty is stronger than inhibitory action of hypotension. There is no research into the correlation between the level of serum sodium and VP, urine sodium and VP, plasma osmotic pressure and VP, urine osmotic pressure and VP.Urotensin-II (U-II) is the strongest vasoconstrictor peptide in vivo to date, and its potency of vasoconstrictor is ten times stronger than endothelin. So far, the research has shown that hU-II levels are significantly increased in cirrhotics compared to controls. In patients with cirrhosis, hU-II levels are higher in ascites than in non-ascites subjects. There has been no research into the correlation between the level of serum sodium and hU-II, urine sodium and hU-II, plasma osmotic pressure and hU-II, urine osmotic pressure and hU-II, so far.Objective: The research predicts observing ascites, hepatic encephalopathy, Child-pugh grading and renal function in different degrees of hyponatremia, understanding the correlation between the damage of liver function and hyponatremia. Acorrding to the research on the correlation between hyponatremia and plasma and urine osmotic pressure, explore the probability of distinguishing between dilutional and low sodium hyponatremia. Meanwhile, determing the level of VP and hU-II of plasma in subjects and probe into the mechanisms of forming hyponatremia and the meaning of determination of VP and hU-II to the diagnosis of hyponatremia.Methods: Select 63 subjects suffered liver cirrhosis and functional disease without disorder of metabolism for water and sodium from No.2 Hospital of Heibei Medical University, Feb.2006 to Jan.2007. Divide 63 subjects into 6 groups by the level of serum sodium. Group A is tested as control group, group B as liver cirrhosis group without ascties, group C as normal sodium group with ascites, group D as slight hyponatremia group with ascites, group E as middle hyponatremia group with ascites, group F as severe hyponatremia group with ascites. Use enzyme linked immunosorbent assay to determine hU-II and VP, Hitachi 7600-020 autoanalyser to determine hepatic function, renal function, urine sodium and urine potassium, PM-8P fully automatic freezing-point osmometer to determine plasma osmotic and urine osmotic pressure, ACL-9000 coagulation analyzer to determine PT (prothrombin time) and APTT (activated partial thromboplastin).Results:1 There are 23 subjects suffered hyponatremia among 55 subjects of liver cirrhosis from No.2 Hospital of Heibei Medical University, Feb.2006 to Jan.2007. Therefore incidence rate of hyponatremia is 41.8%.2 The correlation between hyponatremia and clinic2.1 Hyponatremia and ascites: There are 23 subjects suffered hyponatremia among 46 subjects in liver cirrhosis with ascites; there are 0 subject suffered hyponatremia among 9 subjects in liver cirrhosis without ascites. The significant difference of the number of the subjects between ascites group and non-ascites group can be seen according to correction formula for chi-square test of four-fold table (P<0.05).2.2 Hyponatremia and Child-pugh grading: In 55 subjects with liver cirrhosis, the significant difference among five groups can be seen by Kruskal-Wallis H test of multiple samples (P<0.01). Contrasting any two groups respectively by Nemenyi test, there is significant difference bewteen group B and group E (P<0.05), group B and group F (P<0.01), group C and group F (P<0.01). The result shows in different groups, there is difference in grading of liver function.2.3 Hyponatremia and hepatic encephalopathy: In 55 subjects with liver cirrhosis, the significant difference among five groups in the number of hepatic encephalopathy can be seen by chi-square test of row times column (P<0.01). Contrasting any two groups, there is significant difference between group C and the other groups (P<0.05), group F and the other groups (P<0.05); and there is no significant difference from other results, which may be related to the shortage of samples. The result shows the less serum sodium, the more the number of hepatic encephalopathy.2.4 Hyponatremia and renal function: According to BUN, divide 55 subjects with liver cirrhosis into two groups, group normal BUN(BUN>7.1mmol/L) and group abnormal BUN ( BUN≤7.1mmol/L). In 55 subjects with liver cirrhosis, there is significant difference among five groups by chi-square of row times column (P<0.01). The less serum sodium, the more the number of BUN>7.1mmol/L. Contrasting any two groups, there is significant difference between group F and the other groups (P<0.05), and no significant difference between other groups, in part, for the shortage of samples. The results shows the less serum sodium, the more the number of BUN>7.1mmol/L.3 Hyponatremia and plasma osmotic pressure and urine osmotic pressure and urine-plasma osmotic pressure ratioIn 63 subjects, there is significant difference in plasma osmotic pressure among five groups (P<0.01). Contrasting any two groups, there is significant difference in plasma osmotic pressure except group A and B, A and C, B and C. The less serum sodium, the less plasma osmotic pressure.In 63 subjects, there is significant difference in plasma osmotic pressure among five groups (P<0.01). Contrasting any two groups, there is significant difference in urine osmotic pressure except group A and B, A and C, A and D, B and C, B and D, C and D, E and F (P<0.05).There is no significant difference of urine-plasma osmotic pressure ratio which may be due to influence of many factors for the index.According to correlation test, plasma osmotic pressure is positively correlated with serum sodium (rs=0.909, P<0.01), Urine osmotic pressure is positively correlated with serum sodium (rs=0.592, P<0.01) and no significant correlation between urine-plasma osmotic pressure ratio and serum sodium.4 VP and correlation between VP and hyponatremiaIn group A, B, C, D, E and F, the concentration of VP are respectively (77.03±10.5)pg/ml, (133.24±19.03)pg/ml, (241.21±10.23 )pg/ml, (330.81±34.91)pg/ml, (406.4±13.16)pg/ml, (452.23±15.92)pg/ml. There is significant difference among the groups (P<0.01). Contrasting any two groups, there is significant difference (P<0.05).Serum sodium is negatively correlated with VP (rs=-0.687, P<0.01). 24 hours urine sodium is negatively correlated with VP (rs=-0.899, P<0.01). There is no correlation between urine potassium and VP. Plasma osmotic pressure is negatively correlated with VP (r=-0.837, p<0.01). Urine osmotic pressure is negatively correlated with VP(r=-0.462, p<0.01). There is no significant correlation between urine-plasma osmotic pressure ratio and VP.5 hU-II correlation between hU-II and hyponatremiaIn group A, B, C, D, E and F, the concentration of hU-II are respectively (342.73±26.54)pg/ml, (448.79±44.86)pg/ml, (546.42±14.54)pg/ml, (632.51±40.59)pg/ml, (730.81±35.21)pg/ml, (932.37±28.68)pg/ml. Using one-way ANOVA, there is significant difference among the groups (P<0.01). Contrasting any two groups, there is significant difference (P<0.05).Serum sodium is negatively correlated with hU-II (rs=-0.682, P<0.01). 24 hours urine sodium is negatively correlated with hU-II (rs=-0.885, P<0.01). There is no correlation between urine potassium and hU-II. Plasma osmotic pressure is negatively correlated with hU-II (r=-0.843, P<0.01). Urine osmotic pressure is negatively correlated with hU-II (r=-0.504, P<0.01). There is no significant correlation between urine-plasma osmotic pressure ratio and hU-II.Conclusion:1 The incidence rate of hyponatremia in liver cirrhosis is 41.8%.2 In liver cirrhosis, hyponatremia is correlated with ascites, hepatic encephalopathy, liver function grading (Child-pugh grading) .The poorer liver function, the clearer hyponatremia.3 Hyponatremia is positively correlated with plasma and urine osmotic pressure. The less serum sodium, the less plasma osmotic pressure, the less urine osmotic pressure. Hyponatremia is not correlated with Urine-plasma osmotic pressure. It can not be distinguished between low sodium hyponatremia and dilutional hyponatremia by urine-plasma osmotic pressure ratio which may be due to influence of many factors for the index in liver cirrhosis.4 In liver cirrhosis, the less serum sodiuu, the higher VP and hU-II. The correlation test shows that the increase of VP and hU-II are one of mechanisms of forming hyponatremia and meanwhile they can be supporting index for judgement of hyponatremia.
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